Selectins including CD62 are recognized as vascular adhesion molecules which mediate physiological responses such as immunity, inflammation, and hemostasis. Selectins promote various steps during cancer progression enabling the interactions between tumor cells and the blood constituents. With advanced and high-end technologies, rich experienced scientists, Creative Biolabs is an excellent service provider in the field of tumor marker assay. After long years ahead to fully comprehend tumor marker, we launch our CD62 assay portfolio service which can be useful for targeted cancer therapy and diagnosis.
Selectins, vascular adhesion molecules, are a family containing three C-type lectins expressed by bone-marrow-derived cells and endothelial cells. These molecules are recognized as P-selectin expressed on platelet and endothelial cells, L-selectin expressed on leukocytes and E-selectin expressed on endothelial cells. All of them have a similar structure consisting of one EGF-like domain, an amino-terminal lectin domain, several consensus repeats, a single transmembrane domain and a carboxy-terminal cytoplasmic domain.
Fig.1 Schematic representation of P-, E-, and L- selectin structures. (Tvaroška, 2020)
Fig.2 Selectin-dependent signaling during cancer progression. (Borsig, 2018)
CD62, also known as PADGEM protein, GMP-140 and P-selectin, is found in secretory granules of platelets (α-granules) and endothelial cells (Weibel-Palade bodies). CD62 has been illustrated to bind to multiple cancers and cancer-derived cell lines, including breast cancer, colon cancer, lung cancer including small-cell lung cancer, malignant melanoma, gastric cancer, neuroblastoma, and adenoid cystic carcinoma of the salivary gland.
Studies have indicated that CD62 can play important roles in the growth and metastasis of cancers. For instance, the interaction of activated platelets (CD62-mediated) with cancer cells may locally supply various growth factors and mitogens including platelet growth factors, that promote the proliferation and division of cancer cells in situ. Moreover, several pieces of evidence suggest that the binding of human cancer cells, derived from various organs and/or tissues, including HL-60 cells, NKI-4 cells, NCI-H345 cells, Acc-M cells, to P-selectin may be mediated by very different glycoprotein ligands. P-selectins also binds to heparin and heparan sulfates, which inhibit leukocyte adhesion mediated by P-selectin. Additionally, sulfation is also critically required for P-selectin binding to somatic cancer cells.
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